Drachman D B, Weiner L P, Price D L, Chase J
Arch Neurol. 1976 May;33(5):362-7. doi: 10.1001/archneur.1976.00500050048009.
Immobilization of the embryo has been postulated to cause the joint deformities in arthrogryposis multiplex congenita (AMC). Experimental damage to the motor neurons or pharmacologic blockade of neuromuscular transmission has previously resulted in typical joint changes of AMC. In the present investigation, we have studied the effects of paralysis produced by a viral myopathy on joint development. Coxsackievirus A2 was injected intravenously into chick embryos on the seventh day of incubation. Within 48 hours, severe myositis and paralysis resulted. Electron microscopical and immunofluorescence techniques demonstrated virus in muscle cells. Within three to four days after infection, the muscle had virtually disappeared. Ankylosis of joints, corresponding to that seen in human AMC, occurred. This study shows that primary myopathy with paralysis can produce arthrogrypotic joint deformities. The possibility of a viral etiologic factor in some human cases of AMC should be considered.
胚胎固定被认为是导致先天性多发性关节挛缩症（AMC）关节畸形的原因。先前对运动神经元的实验性损伤或神经肌肉传递的药理学阻断已导致AMC典型的关节变化。在本研究中，我们研究了病毒性肌病导致的麻痹对关节发育的影响。在孵化的第7天，将柯萨奇病毒A2静脉注射到鸡胚中。在48小时内，导致了严重的肌炎和麻痹。电子显微镜和免疫荧光技术在肌肉细胞中发现了病毒。感染后三到四天内，肌肉几乎消失。出现了与人类AMC中所见相似的关节强直。这项研究表明，伴有麻痹的原发性肌病可导致关节挛缩性关节畸形。应考虑在某些人类AMC病例中存在病毒病因的可能性。
